The utilization of many different animal models, all of which have been selected for a high incidence of neoplasia due to an infectious retrovirus, has provided an enormous body of information concerning the induction of neoplasia in both viral and nonviral-induced cancer. We are focusing on three retroviral systems, all of which represent natural field infections (feline leukemia virus, bovine leukemia virus and equine infectious anemia virus) to better understand the molecular events that are responsible for tumorigenesis. We have isolated a new, defective feline virus which has transduced the oncogene myc. DNA sequence analysis of this isolate shows that the transduced myc oncogne is a P-30 fusion product. Proviral formation and transcriptional regulation studies on the bovine leukemia virus indicate that this virus readily forms provirus in a wide range of hosts, but requires host cell factors for a productive infection. These host cell factors are present only in a few cell lines and may be the critical rate-limiting step in the genesis of tumors. The equine infectious anemia virus is under study principally because of an antigenic relationship with the human retrovirus, HTLV-III, which is the principle candidate for the etiologic agent in the acquired immunodeficiency syndrome (AIDS). We have molecularly cloned this isolate and will proceed with nucleic acid hybridization studies to establish if a genetic relationship exists with human retroviruses.